Forty-two patients with patella fracture were treated by nickel-titanium memory alloy patellar concentrator(NT-PC) in Department of Orthopedics,First People’s Hospital of Nanning from August 1994 to February 2004,and antibiotic was applied after operation.No infection or hypersensitive response was found in any case.Bone union occurred in all patients.No dislocation was found.Among 42 patients,37 cases were excellent,3 were good,and 2 were poor.Among 26 patients with comminuted fracture,25 were excellent,and 1 was good.The NT-PC is a good selection of medical implant for the treatment of patellar fracture,especially for comminuted fracture.

【Objective】To investigate the influence of serum containing Hechan Tablets(HT)on the proliferation and apoptosis of human lung adenocarcinoma cell(LAC)line.【Methods】Serum containing HT was prepared.Human LAC line was cultured by the routine method firstly,and then was planted respectively in the culture medium including serum containing HT at the concentration of 30%(group A),in the culture medium including blank serum at the same concentration(group B)and in RPMI-1640 culture medium(group C).The growth of LAC was monitored under inverted phase contrast microscope,histological features of apoptotic LAC nucleus examined under fluorescence microscope and the apoptosis of LAC observed by flow cytometry with the methods of DNA content analysis and terminal-deoxynucleotidyl transferase mediated nick end labeling(TUNEL).【Results】After treatment with serum containing HT,the apoptotic changes of LAC were as follows: apoptotic rate was 5.6% in group A,lower than 0.9% in group B and 0.1% in group C;DNA content analysis showed that the number of LAC which was in phase S and phase G2-M was less in group A than that in groups B and C 72 hours after the culturing,so did the cell proliferation index;the results of TUNEL examination showed that the incidence of cell apoptosis was 12.3% in group A,5.7% in group B and 1.2% in group C 72 hours after the culturing.【Conclusion】Serum containing HT has an inhibitory effect on the proliferation of LAC,and its mechanism may be related to inhibiting DNA synthesis and division of LAC,restraining LAC at the phase G0 and G1 and promoting LAC apoptosis.

In order to research into the relationship between atrial natriuretic peptide (ANP), aldosterone (Aldo) and pregnancy-induced hypertension (PIH), as well as normal pregnancy, the plasma concentrations of ANP and Aldo from normal pregnant women. PIH patients and their fetuses were measured by radioimmunoassay. It was found that maternal venous Aldo and ANP were higher in normal pregnant women than those in non-pregnant women. The plasma ANP was higher in PIH patients than that in normal pregnant women while plasma Aldo was lower. The plasma concentration of ANP was higher in the fetuses of PIH patients than that in the normal controls, but Aldo was lower. It is concluded that ANP concentration correlates significantly to the severity of PIH, and may be used for an early diagnosis of PIH.

Objective To optimize the formulation of metoprolol succinate ( MS) controlled release pellets by central composite design-response surface methodology .Methods MS sustained-release pellets were prepared using sugar pellet cores as starter beads , ethyl cellulose as coating materials and MS itself as a pore former .The formulation of MS sustained-release pellets was optimized by a central composite design with two factors at five levels .These two factors ( two independ-ent variables) were the pore former level and coating level , and the evaluated indexes ( namely dependent variables ) included the in vitro cumulative release percentages of MS at 1, 4, 8, 12 and 16 h, respectively.Results and Conclusion The results of mathematical equation fitting suggested that the second-order quadratic model was the optimal fitting equa-tion.According to the response surfaces , the optimum values at the pore former level and coating level weve ranged from 16%to 18%and 20% to 25%, respectively .The in vitro cumulative release percentage of MS from the pellets at 1 h reached 9.15%,which consequently eliminated the lag phase in the initial release period and exhibited a good sustained-release effect.Central composite design-response surface methodology can be applied to optimizing the coating formulation for MS sustained release pellets .

Cancer is a highly aggressive and devastating disease, and impediments to a cure arise not just from cancer itself. Targeted therapies are difficult to achieve since the majority of cancers are more intricate than ever imagined. Mainstream methodologies including chemotherapy and radiotherapy as routine clinical regimens frequently fail, eventually leading to pathologies that are refractory and incurable. One major cause is the gradual to rapid repopulation of surviving cancer cells during intervals of multiple-dose administration. Novel stress-responsive molecular pathways are increasingly unmasked and show promise as emerging targets for advanced strategies that aim at both de novo and acquired resistance. We highlight recent data reporting that treatments particularly those genotoxic can induce highly conserved damage responses in non-cancerous constituents of the tumor microenvironment (TMEN). Master regulators, including but not limited to NF-kB and C/EBP-β, are implicated and their signal cascades culminate in a robust, chronic and genome-wide secretory program, forming an activated TMEN that releases a myriad of soluble factors. The damage-elicited but essentially off target and cell non-autonomous secretory phenotype of host stroma causes adverse consequences, among which is acquired resistance of cancer cells. Harnessing signals arising from the TMEN, a pathophysiological niche frequently damaged by medical interventions, has the potential to promote overall efficacy and improve clinical outcomes provided that appropriate actions are ingeniously integrated into contemporary therapies. Thereby, anticancer regimens should be well tuned to establish an innovative clinical avenue, and such advancement will allow future oncological treatments to be more specific, accurate, thorough and personalized.
Antineoplastic Agents ; therapeutic use ; CCAAT-Enhancer-Binding Protein-beta ; metabolism ; Humans ; Models, Biological ; Molecular Targeted Therapy ; methods ; trends ; NF-kappa B ; metabolism ; Neoplasms ; drug therapy ; metabolism ; Precision Medicine ; methods ; trends ; Signal Transduction ; drug effects ; Tumor Microenvironment ; drug effects

Objective: To explore the clinical application of individualized design of facial artery perforator flap for the repair of midfacial defect caused by tumor resection. Methods: From January 2015 to January 2018, a total of 36 cases of midfacial defect were repaired by individualized designed facial artery. Flaps were designed and harvested according to the location and size of the midfacial defect resulted from tumor resection, including propeller flaps, droplet flaps and swallowtail-shape flaps. Flap size was between 1.3 cm × 1.6 cm and 2.0 cm × 4.2 cm with the donor site being sutured in the first stage. Results: During the 6 months to 3 years of postoperative follow-up, no tumor recurred. All the 36 cases of individualized designed facial artery perforator flaps survived well. Furthermore, flaps being designed according to the wound defect had a good appearance, the flaps matched the color and texture of the surrounding skin and had a favorable appearance. Besides, flaps had a certain degree of sensory recovery while there was no obvious scarring presented in the donor area. Conclusions Individualized design of facial artery perforator flap has great advantages of simple and flexible, easy manipulation, reliable flap blood flow and minimal donor injury, which render it valuable for clinical application.

Objective:To develop a radiomics nomogram model based on CT to distinguish arteriovenous malformation(AVM) intracerebral hemorrhage from primary intracerebral hemorrhage.Methods:One hundred and thirty-five patients with cerebral hemorrhage confirmed by operation in the First Affiliated Hospital of Soochow University were analyzed retrospectively, including 52 patients with AVM cerebral hemorrhage and 83 patients with primary cerebral hemorrhage. Radiomics features were extracted from baseline CT, radiomics score (Radscore) was calculated and radiomic labels were constructed. Multiple logistic regression analysis was used for clinical features combined with CT signs to establish a clinical model. And then the nomogram model was generated according to the Radscore and the clinical model. The ROC curve and decision curve analysis (DCA) were used to evaluate the discrimination performance of the model.Results:Six features were selected and used to establish radiomic labels. The clinical model consisted of age (OR: 4.739, 95%CI 1.382-16.250) and hematoma location (OR: 0.111, 95%CI 0.032-0.385), while the nomogram model consisted of age, hematoma location and Radscore. In the training group, there was a significant difference between the nomogram model [area under curve (AUC) 0.912] and the clinical model (AUC 0.816), the radiomics model (AUC 0.857) ( Z=2.776, 2.034, P=0.006, 0.042, respectively); While in the validation group, there was no significant difference between the nomogram model (AUC 0.919) and the clinical model (AUC 0.788), the radiomics model (AUC 0.810) ( Z=1.796, 1.788, P=0.073, 0.074, respectively). DCA analysis showed that the clinical value of the nomogram model was superior to the clinical model and radiomic model. Conclusion:The radiomics nomogram can effectively distinguish AVM-related cerebral hemorrhage from primary cerebral hemorrhage, which is helpful for clinical decision-making.

Objective To summarize the core prescription for treating metabolic syndrome by academician TONG Xiaolin and explore the intervention mechanism.Methods Outpatient medical records of TONG Xiaolin's treatment for metabolic syndrome were input into the Ancient and Modern Medical Records Cloud Platform for data mining,then the core prescription was extracted.The effective components and therapeutic targets of the core prescription,and metabolic syndrome-related genes were obtained from relevant databases.The core targets were screened out by protein-protein interaction network.The network of core prescription-core compound-core target was constructed.Pathway enrichment analyses were carried out based on the core targets.Results A total of 1 028 records were enrolled and analyzed.The core prescription consists of 10 Chinese medicinals,such as Coptidis Rhizoma,Anemarrhenae Rhizoma,Paeoniae Radix Rubra,etc..The prescription was modified with three-herb formulas,which was composed of Fritillariae Thunbrgii Bulbus,Curcumae Rhizoma and Notoginseng Radix et Rhizoma.A total of 151 active compounds and 64 potential targets for metabolic syndrome of the core prescription were obtained.The core compounds included isorhamnetin,calycosin,berberine and monacolin K.The core targets were MAPK3,MAPK8,and LDLR.The PI3K-Akt,AGE-RAGE and MAPK signaling pathways were involved.Conclusion The core prescription of academician TONG Xiaolin's treatment for metabolic syndrome was composed of Coptidis Rhizoma,Anemarrhenae Rhizoma.The prescription was modified according to symptoms in the form of three-herb formulas.The core prescription may exert its effect by regulating PI3K-Akt,AGE-RAGE,MAPK and other signaling pathways,which could reflect the characteristics of Chinese herbal compound,such as multi-component,multi-target,multi-pathway,and comprehensive regulation.

Objective:To identify the pathogenic gene of a pedigree with symphalangism and to prove the pathogenicity of this locus in vitro.Methods:The clinical data of patients’families were collected at Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, peripheral blood was collected and genomic DNA was extracted and NOG, FGF9, GDF5 exon regions were amplified by PCR, and the exon gene mutations were detected by first-generation sequencing technique. The structure of noggin-GDF5 protein complex was simulated in silicon. COS-7 cells were transfected with 5 μg empty plasmid, wild type plasmid and V202G mutant plasmid in vitro. Each group of plasmids was transfected into 3 well cells. The experiment was repeated for 3 times, and the expression of noggin protein was detected by Western blotting. C2C12 cells were also transfected with the above plasmids in vitro for osteogenic differentiation. By applying alkaline phosphatase staining and quantitative assay. Relative expression level of osteoblast-related genes Col1α1, ALP and Runx2 were detected by qRT-PCR. Each group of plasmids was transfected into 3 well cells, and the experiment was repeated for 3 times. All statistical analysis were performed by Prism 6 software. The result were shown as mean±standard deviation, and the comparison between groups was done by unpaired t-test. Data were considered statistically significant when P value is less than 0.05. Results:Both the proband and his mother suffered from symphalangism. The result of Sanger sequencing showed that there was a heterozygous missense mutation of NOG gene (p.V202G) in all patients in this pedigree. No disease-related mutations were detected in FGF9 and GDF5. Computer three-dimensional mechanism simulation showed that the site was located at the α helix. The result of Western blotting showed that the expression of mutant protein was significantly lower than that of wild type. Osteogenic differentiation in vitro showed that the inhibitory effect of V202G mutant protein on osteogenic differentiation decreased. The quantitative result of alkaline phosphatase staining showed that the alkaline phosphatase activity in the vector group was (12.3±0.8) U/L, and the alkaline phosphatase activity in the wild type plasmid group was (2.6±0.3) U/L, which was significantly lower than that in the vector group ( t=11.550, P<0.001). The alkaline phosphatase activity in the mutant plasmid group was (10.8±0.3) U/L. There was no significant difference between the mutant group and the vector group ( t=1.830, P=0.141). The mRNA expression level of osteogenesis-related genes was consistent with the above result . Compared with vector group, the expression of osteogenesis-related genes in wild-type noggin group decreased significantly ALP、 Col1α1 and Runx2 ( t=5.987, 4.498, 4.170; P=0.004, 0.011, 0.014). There was no significant difference between mutant plasmid group and blank vector group in ALP、 Col1α1 and Runx2 ( t=0.433, 0.177, 1.159; P=0.688, 0.868, 0.311). Conclusions:NOG gene c. 605T < G p. V202G is a novel mutation in symphalangism, which is located in the α helix of noggin protein, leading to the decrease of the expression of noggin protein and the manifestation of ankylosis.

Objective:To identify the pathogenic gene of a pedigree with symphalangism and to prove the pathogenicity of this locus in vitro.Methods:The clinical data of patients’families were collected at Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, peripheral blood was collected and genomic DNA was extracted and NOG, FGF9, GDF5 exon regions were amplified by PCR, and the exon gene mutations were detected by first-generation sequencing technique. The structure of noggin-GDF5 protein complex was simulated in silicon. COS-7 cells were transfected with 5 μg empty plasmid, wild type plasmid and V202G mutant plasmid in vitro. Each group of plasmids was transfected into 3 well cells. The experiment was repeated for 3 times, and the expression of noggin protein was detected by Western blotting. C2C12 cells were also transfected with the above plasmids in vitro for osteogenic differentiation. By applying alkaline phosphatase staining and quantitative assay. Relative expression level of osteoblast-related genes Col1α1, ALP and Runx2 were detected by qRT-PCR. Each group of plasmids was transfected into 3 well cells, and the experiment was repeated for 3 times. All statistical analysis were performed by Prism 6 software. The result were shown as mean±standard deviation, and the comparison between groups was done by unpaired t-test. Data were considered statistically significant when P value is less than 0.05. Results:Both the proband and his mother suffered from symphalangism. The result of Sanger sequencing showed that there was a heterozygous missense mutation of NOG gene (p.V202G) in all patients in this pedigree. No disease-related mutations were detected in FGF9 and GDF5. Computer three-dimensional mechanism simulation showed that the site was located at the α helix. The result of Western blotting showed that the expression of mutant protein was significantly lower than that of wild type. Osteogenic differentiation in vitro showed that the inhibitory effect of V202G mutant protein on osteogenic differentiation decreased. The quantitative result of alkaline phosphatase staining showed that the alkaline phosphatase activity in the vector group was (12.3±0.8) U/L, and the alkaline phosphatase activity in the wild type plasmid group was (2.6±0.3) U/L, which was significantly lower than that in the vector group ( t=11.550, P<0.001). The alkaline phosphatase activity in the mutant plasmid group was (10.8±0.3) U/L. There was no significant difference between the mutant group and the vector group ( t=1.830, P=0.141). The mRNA expression level of osteogenesis-related genes was consistent with the above result . Compared with vector group, the expression of osteogenesis-related genes in wild-type noggin group decreased significantly ALP、 Col1α1 and Runx2 ( t=5.987, 4.498, 4.170; P=0.004, 0.011, 0.014). There was no significant difference between mutant plasmid group and blank vector group in ALP、 Col1α1 and Runx2 ( t=0.433, 0.177, 1.159; P=0.688, 0.868, 0.311). Conclusions:NOG gene c. 605T < G p. V202G is a novel mutation in symphalangism, which is located in the α helix of noggin protein, leading to the decrease of the expression of noggin protein and the manifestation of ankylosis.